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MIT HST 121 - Study Guide

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1 December 2005 HST 121 Gastrointestinal Pathophysiology Sections between Midterm and Final. A few general comments... 1. Typically, the final exam is much more clinically oriented than the midterm exam. It is also longer and more difficult. 2. Therefore, make sure you study the minicases & clinics very thoroughly, and try to integrate this material with what you learned in the sections & labs. 3. The main subject of the post-midterm part of the course has been the liver, along with the pancreas and biliary tract. I recommend skimming/reading parts of Lippincott’s Illustrated Review of Biochemistry (by Champe & Harvey) since much (if not most) of liver physiology is really biochemistry. 4. Please know and understand your classmate’s questions. Dr. Carey may change these a bit, but many of these will be on the exam. 5. Email me if you have any questions ([email protected]). Harvard-MIT Division of Health Sciences and TechnologyHST.121: Gastroenterology, Fall 2005Instructors: Dr. Martin Carey, Dr. Raymond Chung, Dr. Daniel Chung, and Dr. Jonathan Glickman2 Section 11: Lipids (Carey) Focus on application of these ideas to biology (eg., plasma & intracellular membranes, lipoproteins). 1. You should know the basic categories of lipid systems (both single & mixed) and be able to give biological examples wherever possible. Important ones include:  liquid crystals/mesophases (lyotropic and thermotropic formation)  micelles include bile salts  mixed liquid crystals include cell and organelle membranes, biliary mixed vesicles  these are lamellar liquid crystals, which means that the lipids can move freely only in the two dimensions within the plane of the lamella  mixed micelles include biliary mixed micelles  stable emulsions (dispersions of lipid in lipid) include plasma lipoproteins, dietary fat 2. Understand the difference in behavior between nonpolar and polar lipids. Basically:  nonpolar lipids form oils  polar lipids can interact with aqueous solvents in various ways:  insoluble, non-swelling: alone, form crystals or oil droplets; found in mixed micelles, membranes (cholesterol); function as emulsifiers  insoluble, swelling: form liquid crystals (phospholipids that make membranes), found as emulsifiers in lipoproteins  soluble: form micelles; example is bile salts 3. Know the three “P” rules.  Predictability rule: you can predict the physical form of a lipid in a biological system if you know how the lipid behaves in an aqueous system.  Predominance rule: the majority lipid will govern the behavior of the system  Phase rule: F = C - P + 2, where F=degrees of freedom (variance), C=number of components (order), P=number of phases.  Basically, if you have a system, you count up how many chemical constituents there are (C) and how many phases there are (liquid, gas, solid, liquid crystal, etc.). This tells you F, which is the number of variables you can change without changing the properties of the phases or constituents. The possibilities for F are temperature, pressure, and concentration. 4. Know the basics of examples of biologically relevant lipid systems.  Cholesteryl Esters: biological variations in temperature can change their phase from crystal to liquid crystal to oil. They are the major kind of cholesterol in blood.  Cholesterol/Water: think of gallstones and atherosclerosis  Phosphatidylcholine (lecithin)/Water: think of model membranes/vesicles  Bile Salt/Water: remember from above_forms micelles  Cholesterol/Lecithin/Water: cell membrane. Note: there is a small region of the system’s phase diagram where the lamellar liquid crystalline phase can exist by itself. This establishes the boundaries for concentrations physically allowed within the cell membrane; ratio of 1:1 cholesterol:lecithin is upper limit.  Bile Salt/Lecithin/Cholesterol/Water: models both gallstones and fat digestion depending on which part of the system’s phase diagram you look at.3 5. Biomembranes: a few things to point out.  Notice the amount of cholesterol in different membranes: mammalian plasma membranes contain up to 1:1 cholesterol:lecithin but organelles have little.  Roles of lipids in membranes include:  structure; eg., caveolae, which are plasma membrane domains of specific lipid composition  second messengers; eg., IP3, PIP2, DAG  anchors for membrane proteins Different lipids are in inner/outer membrane leaflet. PS, PI, PE are inside; PC, glycosphingolipid, gangliosides are outside. When a cell (eg., RBC) is senescent, amino phospholipid flipase stops working, allowing PS to flip slowly from the inner to the outer leaflet, signalling for destruction. 6. Lipid movement  across membranes  as single molecules: rely on passive diffusion, facilitated diffusion, coupled transport, active transport. Eg: bile salt transporters in enterohepatic circulation (see Section 15)  as aggregates: endocytosis (eg, LDL endocytosis) or scavenger receptors (eg, HDL internalization) play roles here.  in liquid. Eg: lipids are carried inside lipoprotein emulsions in plasma (see section 19) Section 12: Physiology & Biochemistry of Exocrine Pancreas (Freedman) The exocrine pancreas secretes digestive enzymes, bicarbonate, mucin, and water into the duodenum.  Acinar cell secretes zymogens and enzymes.  Centroacinar and intralobular duct cells secrete bicarbonate and water.  Interlobular and main duct cells secrete bicarbonate and mucin.  Bicarbonate needed for zymogen solubility & apical membrane trafficking in acinar cell 1. What does the acinar cell secrete?  Trypsinogen, chymotrypsinogen, proelastase, carboxypeptidases digest peptides.  Amylase begins breakdown of amylose & amylopectin yielding maltose & maltotriose.  DNAse, RNAse  Elastase, collagenase, phospholipase  Pancreatic Lipase, which requires colipase. 2. How is the pancreas protected from these destructive enzymes?  Before secretion, enzymes are in membrane-bound compartments separate from lysosomal enzymes. Acidity of compartments inactivates trypsin.  Enzymes are secreted as inactive precursors (zymogens) that require enterokinase, released from duodenal mucosa, as a trigger. Enterokinase needs Ca++, which is lacking4 in the pancreatic ducts.  Trypsin inhibitors (PSTI) and degraders


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